Providing straightforward information pertaining to drugs, drug use & drug policy. The Grey Pages promotes drug-related literacy and advocates a system of viable and tolerant drug policies. This is my personal collection of commentaries, essays, tid-bits, and other such writings on everything ranging from drug use, drug policy and drug-myths, to drug-science, addiction, human behavior, and the workings of the human brain. I started this blog with a particular focus on opioids, and over the past year have found my interest gravitate toward the intriguing, ever-changing world of designer intoxicants (i.e. "research chemicals" or "designer drugs").

Sunday, January 30, 2011

Oxymorphone & Hydromorphone in Hospital Emergency Medicine

Bad shit happens. Auto accidents, kidney stones, myocardial infarctions, cluster headaches and broken bones leave the injured in agonizing pain and most likely a trip to a hospital emergency department.

American Physicans tend to be predominantly drawn to the use of morphine in these situations. Morphine, the simple solution, right? Doctors seem to greatly overestimate the power of morphine, and especially the tolerability.


The highly potent and often superior opioids hydromorphone and oxymorphone are very under utilized medicines for this purpose.

In acute management of sudden pain, such as the emergency room setting, 1mg of oxymorphone IV is equivalent to 12.5mg of oxycodone orally; a good dose for a non opioid addict in severe pain such as broken bones or severe injury. Injected directly to the bloodstream however, the oxymorphone will have immediate effect, releiving pain within 10 to 15 seconds and alleviating the suffering of the injured. The effect is amazing to watch first hand; a badly injured person writhing in agony one moment, and within an instant, all tension released, heavy breathing becomes gradual, blood pressure returns to normal, and the patient melts away into a warm, euphoric state of comfort.

Potent morphine derivatives like oxymorphone and hydromorphone give equivalent pain relief to morphine, only in much smaller doses and volumes; not to mention, these newer derivatives cause much fewer side effects in most people. Where morphine leaves a patient often itching and vomiting, Numorphan or Dilaudid are far less prone to these effects. Physicians are somewhat ignorant regarding the superior properties, and better suitability of more modern/refined drugs than morphine. It frustrates me that these Doctors widely still honor morphine as the "King", the gold standard. Giving it to virtually everyone as the first-line, first-choice. In large part due to it's very old age.

Nitrous Oxide Vault

(Also known as N2O, nitrous, or laughing gas)

N2O is a gaseous oxide of nitrogen. It has a variety of applications ranging from aerosol spray propellant, to rocketry or car engine oxidation agent. It is commonly used as a medical or dental anaesthetic and recreational drug. It is administered through inhalation.

Nitrous oxide is known to exhibit multiple actions on the central nervous system - first and foremost, it blocks the NMDA receptor. It also demonstrates anticholinergic activity (blocking the beta-2 nicotinic subtype). Also reported are its inhibion of AMPA, GABA-C, and 5HT3 receptors; and positive modulation of GABA-A receptors (i.e. BZD receptors).

"Protecting The Children" As A Justification for Drug Laws

Consider The Following:

A) It is easier for children to obtain marijuana or prescription-only narcotics than it is to obtain alcohol.

B) Children are taught from a ripe young age to abstain from drug abuse & underage drinking. Any children who drink are well aware they are breaking the law.

C) Tobacco & alcohol use by minors is illegal; It is nonsensical to believe that casual narcotic use by minors would be any exception were they to be legalized.

D) Any parent who allows a child to get shitfaced or is unaware of a childs drinking & drug use is an incompetent parent and should have their child given to new parents who will instill law-abiding values and discipline in their children.

E) People of the free world are not obligated to sacrifice their most intimate personal rights in order to save others the trouble of responsibly parenting their own children, much less to spare others the trouble of suffering consequences of their own potentially poor choices.

Friday, January 28, 2011

Drug Use is Never Involuntary

It is very important to understand that just the fact that a certain behavior is influenced by changes in the brain, does not make the behavior involuntary.

Consider this excerpt, quoted from an “addict in recovery” - “Addiction makes all of us do things we would never have dreamed of".

Herein lies the problem. Addiction does not “make” anyone do anything.

These behaviors being referred to are not involuntary, nor are they beyond our control. Addiction often leads the affected person to do things they would’ve previously never imagined they would do because the brain has adapted to prioritize drugs in the same way it prioritizes food and water. This doesn’t necessarily cause the addict to behave in any certain fashion, but it creates an emotional disposition in which doing so might seem more appealing, or even essential, thus making it more likely that the addict will choose to behave in a fashion which accomodates his every whim to the detriment of other values or priorities in his life.

Addiction affects our emotional disposition and feelings, whereas we as individuals are left to rationally analyze these feelings and to choose our behaviors accordingly. Feelings, emotion, and instinct must be differentiated from behavior - yet in the case of the disease model of addiction, these two very distinct factors are incorrectly conceptualized as one in the same.

Being human, we take comfort in believing that those who continue to use drugs despite negative consequences really don't want to be doing so, but can not control this behavior because they are the victims of a medical affliction, a disease which causes them to use drugs recklessly and involuntarily. This is, unfortunately (or perhaps fortunately, depending on ones perspective), not the case.

Let’s use the analogy of the motorcross racer - most of these individuals love to race their dirtbikes, so much in fact that they will continue to race and ride in spite of multiple accidents, serious injuries, and near death experiences. Furthermore, their racing of dirtbikes has led to changes in certain areas of the brain associated with this particular activity.

Many people in the profession of extreme sports are not deterred by the prospect of death, and in fact they would be happy to die doing what they love. Is their incessant passion for extreme and dangerous sports, along with the associated changes in their brains, indicative of a disease which causes involuntary behavior? Does their continuation of dangerous sports despite broken bones and the risk of death indicate they are not in control of their behavior?

Perhaps the pro motorcross racer wants badly to stop racing, but he simply cannot resist, and, is compelled to climb on his bike involuntarily at the sight of a racetrack..

Sound a bit ridiculous? That's because it is.

Monday, January 24, 2011

Chloral Hydrate Vault

Chloral hydrate is a CNS depressant related to ethanol. It is one of the oldest sedative-hypnotic drugs known, first produced in 1832 by the chlorination of ethyl alcohol. It is used as a short term sleep aid and as a procedural sedative or anaesthetic. Chloral hydrade is believed to act via enhancing the GABA system. Repeated use may lead to dependence and tolerance. The drug is classified as a schedule IV controlled substance. 

Thursday, January 20, 2011

Cocaine: Drug Information


Cocaine is a psychostimulant drug of the tropane family, used for both its psychoactive and its topical anaesthetic properties. It is a naturally occurring alkaloid derived from coca leaf (leaf of the coca bush), which is widely grown (both naturally and commercially) in the mountainous climates of South America. 

Mode of Action

Cocaine is a sympathomimetic psychostimulant. It produces its effects by increasing synaptic concentrations of dopamine, norepinephrine and serotonin; in large part via inhibition of monoamine transporters. Its anaesthetic effect is due to its sodium channel blocking properties.


On the illicit market, cocaine is available in various forms. Pure cocaine itself is typically a hydrochloride based salt (cocaine hydrochloride), a fine, white, flaky, crystalline powder. Street cocaine is rarely available in pure form, and may occur as the following:

Regular Powder - A semi-diluted cocaine hydrochloride powder. The powder is often taken by the intranasal route (snorted); dissolved in water and injected; or to a lesser extent smoked, but with limited success, as the hydrochloride powder only vaporizes at the high temp of 197 celsius and is largely destroyed at this temperature. Cocaine hydrochloride has been taken orally in capsule or parachute form, or applied to the genitals (tip of the penis or trans-vaginally) for surface absorbtion. Diluting agents often present in powder cocaine include baking soda, sugars, and local anaesthetics, the latter of which help enhance the products numbing properties and give the illusion of greater purity.

Freebase - The perfectly pure "base" form of cocaine, in which the compound is not incorporated into any salt (i.e. hydrochloride). Cocaine base may appear as a chunky, white to off white solid (rock or powder) with a shiny or pearly appearance. It is virtually insoluble in water, and poorly absorbed by mucous membranes, therefore it is most often smoked.

Crack - Crack cocaine is a crude form of cocaine base, most often smoked. It has a higher purity than cocaine powder but less so than freebase - crack is sometimes referred to as "dirty base". Crack is produced via neutralization of cocaine hydrochloride in the presence of sodium bicarbonate (baking soda) and water, when heated. The process is so simple that many users produce their own. The final product is an off white solid, usually with a waxy or soap-like quality (in fact, bar soap has frequently been sold as crack); consisting of a mixture of cocaine base, sodium carbonate, water and other impurities. Its name is rooted in the fact that it makes a distinct crackling sound when heated and smoked.

Route of Administration 

Cocaine is short acting drug. Effects generally last 15 to 30 minutes (or longer), depending on the route of administration.

Oral - Orally administered cocaine takes effect after 30-40 minutes and peaks after an hour. Oral use provides the longest duration of effects, but only a portion of an oral dose is absorbed systemically.

Intranasal - Snorted cocaine takes effect relatively quickly; about 5 to 10 minutes is common. About 30-60% of a given dose is absorbed by this route; higher doses and higher concentration lead to better absorbtion. Effects peak aft around 15 minutes and last 30-45 minutes.

Inhalation: Smoking cocaine is the fastest way to get the drug to the brain. It offers a high bioavailability as well (~70%). Effects are felt in seconds, and peak subjective effects have been reported after 1-2 minutes of inhalation - the result is intense and shortlived, lasting only 10-15 minutes. Smoked cocaine, espcially freebase, is believed to be cardiotoxic.

Trans-Tissue Absorbtion: Cocaine may be applied to one of a number of body surfaces for absorbtion. It is often taken this way for its local anaesthetic properties. Users have applied cocaine to the genitals (tip of the penis or vaginally), or to the gums, inner cheek or tounge. Some who apply the drug to the genitals do so to enhance or otherwise affect sexual intercourse and orgasm.

Subjective Effects

Acute effects of cocaine are similar to other psychostimulants.

Increased alertness and wakefulness.

Increased mental clarity.

Euphoria, a sense of well being.

Increased self confidence.

Talkativeness and sociability.

Feelings of empathy or affection toward others.

Increased motivation.

Physiological Effects 

Cocaine arouses the sympathetic nervous system and excites the hypothalamic pituitary adrenal axis. This leads to a fight or flight like state, characterized by increased heart rate, dilated pupils, tunnel vision, vasodilation in vital areas w/ vasoconstriction in nonvital areas, and increased skeletal muscle tone.

Adverse Effects 

Cocaine toxicity can be life threatening. Acute adverse effects include anxiety and panic attack, stimulant psychosis, palpitations, high blood pressure, increased heart rate, cardiac arrhythmias, cardiac arrest and death.

Adverse effects of chronic use include tolerance, psychological dependence, chemical imbalance, loss of appetite, and potential for precipitation of underlying psychotic disorders. Being known to potentiate the mesolimbic dopamine pathways, similar to other rewarding and reinforcing drugs, heavy cocaine use is often associated with addiction. On the other hand, cocaine does not produce the level of physical dependence associated with other drugs such as narcotics and sedative-hypnotics. Cocaine withdrawal is for the most part psychological in nature, and characterized by depression, cravings for cocaine, insatiable appetite, fatigue, amotivation, and oversleeping.

The limbic system may take some time to restore itself, leading to a protracted state of anhedonia (i.e. an inability to experience pleasure), a form of post acute withdrawal syndrome which is common particularly with psychodependence (i.e. "addiction").

Tuesday, January 11, 2011

Methadone and Buprenorphine Maintenance Treatment - Overview

Buprenorphine: HDB

High dose buprenorphine or HDB for short - involves the daily use of the opioid mixed agonist/antagonist buprenorphine in a 1 to 32 milligram dose range, to aid in promoting long term abstinence from traditional opioid agonists. The primary ends of HDB with Suboxone or Subutex are as follows:

1) To attenuate opioid withdrawal symptoms; by attatching tightly to opioid receptors and activating them partially thus providing some degree of narcotic effect. Using an agonist-active opioid such as buprenorphine as opposed to an opioid receptor blocking compound such as naltrexone, is more likely to incentivize compliance on the part of the 'patient', increasing the likelihood that he or she remains in "treatment" and continues taking the medication.

2) To reduce or block the effects of other opioids the subject may be likely to administer; buprenorphine attatches itself so strongly to the opioid receptor that most narcotics are unable to bind in its place, and are therefore less likely to produce effects. 

Buprenorphine, as I've discussed in previous entries, does not produce opioid tolerance past a certain level (specifically about 30mg methadone equivalent) due to its partial agonism and pharmacological ceiling. So unlike methadone, dose increase is not necessary past a certain level. This is a crucial consideration, as even after an extended period of use, there is no mechanism of diminishing returns (or clinical tolerance) to incentivize subjects to increase their dose. The law of diminishing returns experienced by those using opioid agonists often reinforces the compulsive pattern of dose escalation exhibited by many narcotic users.

Methadone: MMT

MMT (Methadone Treatment) is popularly assosiated with heroin addiction. This is increasingly no longer the case, and the assumption is for the most part false. Methadone is used to maintain addiction to various opioids; including morphine, heroin, oxycodone, hydromorphone, fentanyl, etc. MMT has been the classic clinical approach to serious narcotic addiction for over 40 years now, and is based on the principles of "harm reduction" and the "addictive disease" model. Like buprenorphine maintenance, MMT is beneficial in that it offers a socially legitimized means of maintaining a narcotic dependent lifestyle without fear of prosecution.

Methadone Maintenance Treatment, or MMT for short - involves the daily use of the opioid agonist methadone, to promote a reduction in high risk opioid use, particularly by the intravenous route. The ultimate ends of methadone maintentance treatment are as follows:

1) To keep opioid withdrawal symptoms at bay while reducing physiological or emotional craving for other opioids by providing a consistent degree of narcotic effect. Methadone is a mu opioid full agonist with effects similar to similar morphine and heroin.

2) To create a state of hyper tolerance (increased opioid tolerance to an excess point) - This reduces the risk of a fatal overdose in the case that a subject takes other opioids, and serves to disincentivize supplemental drug use by attenuating most of the "rush" produced by other narcotics. At doses of 40 to 70mg or greater, methadone inhibits the euphoric effect opioids taken by the intravenous route - Think of it this way; with methadone already saturating the brain's mu opioid receptors in excess and producing a relatively strong degree of narcosis itself, the introduction of heroin to the brain will do little to increase the current state. A 'rush' is perceived typically when opioid receptors rapidly change from a state of vacant non-activity to a state of moderate to full activity. In addition, as previously explained, tolerance has been increased by the methadone to the point that the typical dose of heroin or morphine would have little effect either way.

Additionally, the pharmacokinetic properties of methadone contribute to its blocking abilities - Taken in high doses, methadone may completely saturate available mu opioid receptors; due in part to its structural characteristics and its particlarly extensive lipophilic distribution. With all opioid receptors occupied and maximally activated, the addition of heroin or morphine is unlikely to produce any additional morphinomimetic effect.

Methadone, being a typical opioid agonist, will produce a steady level of tolerance which will continue to increase over time with each increase in dose. The need for upward dose escalation is perpetual, infinite. The primary problem this presents in my eyes would be; in the case of the dose ceilings that certain clinics or doctors have in place by their own policy. Fortunately, these limitations have become less common over time, and it is common to see patients on doses upwards of 300mg daily.

The decision to discontinue MMT should be reached mutually between the patient and the physician. MMT should be viewed as a means of long term palliation or "harm reduction" rather than a curative measure or even a "treatment". 

Regarding discontinuation of MMT, the product literature for methadone (Mallinckrodt) says the following:

"For Medically Supervised Withdrawal After a Period of Maintenance Treatment There is considerable variability in the appropriate rate of methadone taper in patients choosing medically supervised withdrawal from methadone treatment. It is generally suggested that dose reductions should be less than 10% of the established tolerance or maintenance dose, and that 10 to 14-day intervals should elapse between dose reductions. Patients should be apprised of the high risk of relapse to illicit drug use associated with discontinuation of methadone maintenance treatment."

Methadone VS Buprenorphine - Pros & Cons

Each appoach has its relative advantages and disadvantages. A choice between methadone or buprenorphine should generally not be based exclusively on an individual's tolerance level, however; buprenorphine may or may not provide sufficient attenuation of withdrawal in IV drug users, or in cases of severe dependence to potent opioids such as oxymorphone or fentanyl.

In terms of convenience, buprenorphine may provide a favorable option especially to those living in isolated areas without nearby methadone clinics. 

Buprenorphine is able to be prescribed in an office based, outpatient setting - for example, a family physician, psychiatrist, or internist; where as Methadone as a class II drug is highly regulated, and only authorized for us in a specially licensed facility such as a 'Methadone Clinic' - With new patients required to visit the clinic daily for each dose; and even after a solid patient history has been established, patients may recieve no more than 1 to 2 weeks worth of 'take home' medication with each visit (federal law puts the max supply at 30 days).

Treatment using buprenorphine may appeal to its own particular demographic due to the obvious fact that visiting a doctors office does not carry the stigma or stereotype of waiting in line at a methadone clinic.

Treatment with buprenorphine tends to be more expensive than the methadone route; Physicians who offer HDB often charge substantial fees, both for the initial visit and for subsequent regularly scheduled visits. Some Doctors require patients to visit the office bi-weekly or even weekly in some cases during the first several months of HDB; there is likely of course a profit motive in this.

Methadone is very cheap to manufacture and has been on the market for nearly 100 years, with a number of brand name and generic forms available in the US (and around the world). Prices of MMT tend to be lower than those of HDB treatment; though many methadone maintenance patients recieve treatment through Medicaid or by other federal/state funded means. 

Suboxone - The buprenorphine/naloxone preparation - has yet to see a generic released, and this is not likely to happen anytime soon.

Opioid Agonists and Their Place in Treatment - My Own Beliefs

The Views Discussed herein are product of my own personal opinion and experience, and should be interpreted as such. I base my claims on personal experience and clinical or scientific knowledge, rather than the arbitrary dictates of religious morality or sociopolitical bias.

Opioid Agonist Therapy Should Be Considered For:

For moderate to severe chronic pain that has been resistant to acetaminophen and NSAID's. 
For severe major depressive & anxiolytic disorders which have not responded to conventional treatments & pharmacotherapy; many of these subects may have a history of 'self medicating' using opioids, or may report that opioids have relieved symptoms in the past. 

Single entity-long acting opioids should typically be used in the treatment of psychic distress, in order to achieve steady plasma level & lead to a more stable emotional state. Gradually acting opioids additionally tend to have lower propensity for patterns of problematic use.

This option is to be discussed in depth with patients, and all risks/benefits must be disclosed, including the factor of clinical tolerance, clinical dependence and possible development of narcotic addiction. Discuss withdrawal syndrome upon discontinuation, and the difference between clinical dependence and addiction.

Opioid therapy should be seen as a supportive & palliative measure rather than a curative treatment; and when possible should be prescribed alongside primary forms of treatment such as Osteopathic Manipulative Therapy, acupuncture, physical & behavioral therapy, excersice & healthy diet, and other lifestyle changes. Peripheral nerve blocks & surgery may be an option in some cases; taking into consideration the risk-benefit ratio as well as the original objectives of treatment and financial concerns. The patient's desires concerning direction of treatment and goals/objectives will always be put first and foremost; physicians shall provide patients insight, guidance and support possible regarding their medical conditions, medications, and treatments, while disclosing all potential risks and side effects (especially concerning the addictive qualities of narcotic analgesics).

Hydrocodone and Acetaminophen & Oxycodone and Acetaminophen: These are common first line narcotics; they can be initiated at 1q6-8h doses, taken as needed - however patient preference or clinical requirement may eliminate the option of acetaminophen due to hepatic toxicity concerns. Likewise, oral NSAIDs are contraindicated in patients with a history of GI issues & peptic ulcers. In these cases, avoid combination analgesics (Vicodin, Percocet, Lortab).

Opioids should be started on an 'opioid trial' basis. Choice of analgesic should be based upon the patient's severity of symptoms, intensity of symptoms, frequency & duration of symptoms, overall health of the patient, physiological & metabolic factors, and patient preference. 

Patients should be regularly assessed for overall response & possible toxicity. Dose should be titrated (raised or lowered) according to response during the trial period. The need for opioids should additionally be reassessed periodically.

After a succesful trial of short acting opioids, being 4 weeks or more, a long acting formula can be prescribed for 24 hour baseline analgesia. An additional short acting opioid may be given alongside for supplemental analgesia or sudden onset pain. Preferred long acting opioids include OxyContin & MS Contin, Avinza & Kadian, Opana ER, Duragesic, Exalgo, as well as Methadone.

Monday, January 10, 2011

The Low Down - Methadone

If you're getting you methadone from friends/dealers:

Comes in 5mg and 10mg tablets. 40mg diskettes are less common but still out there; used in the city clinics.

This stuff is extremely strong for the uninitiated. No more than 5mg for a first time user. As little as 10mg (one tablet) could kill someone with low tolerance.

Due to the high volume of distribution, methadone is long acting. Additionally, it takes a long time for effects to kick in; as long as 2 to 3 hours should be expected. Don't take more after an hour or two thinking it wasn't enough, just wait. Trust me.

When it does kick in, it comes on strong and hard, hits like a warm ton of bricks and continues to grow in intensity for several hours til peak.

The itchies tend to be present with methadone, don't scratch yourself til you bleed.

Euphoria is strong with methadone, especially in the beginning. Energy and motivation are usually greatly enhanced. Euphoric qualities will dissipate with tolerance, however returns with a higher dose. Tolerance to methadone grows slower than with other opioids.

Cold weather will become a non issue; you'll have no sensitivity really to the cold, however heat will be amplified. Methadone + Heat = Sweating

Nausea and vomiting is to be expected, especially for anyone who is not opioid dependent - meaning, a heavy habitual user. If vomiting bothers you, you just may want to reconsider whether narcotics are really for you. It takes time but you will get used to it. Many junkies enjoy the vomits as part of the high, part of the experience - Puking = Good dope, You're high

Sedation will become heavier several hours in. If you're not familiar with the state of "Nodding out", you'll quickly learn. The twilight sleep state is common with methadone for some, at least in the beginning.
If you're breathing heavily or having respiratory trouble, don't fall asleep or lie down. Get to an Emergency Room a.s.a.p. Methadone has a strong tendency to cause respiratory depression; the hallmark of narcotic overdose. Don't be another coroner's statistic.

Overall effects of methadone are equivalent in origin to morphine; but stronger due to the high tissue absorbtion of methadone. Very similar to high doses of injected morphine.

If you're getting your methadone through a clinic:

Most clinics I've been to or know of use the cherry flavored liquid. Your daily dose is pumped out, with a machine measuring the exact amount; then diluted in water. It looks and tastes like pink liquid benadryl. You drink your dose in front of the nurse behind the counter.

Methadone Clinics in Michigan are limited to the southern area of the state; Detroit and surrounding areas, Kalamazoo, Muskegon, Grand Rapids, Lansing, etc. Prices in Michigan vary, most clinics take cash or Medicaid. I've only been to clinics in NYC, which universally take medicaid; unless you want to fork out 180.00$ weekly in cash; which is the rate at the Beth Israel Clinics. Beth Israel sponsors at least a dozen clinics throughout Manhattan and the surrounding burroughs.

Typically you'll start out at 30mg on the first day or two, then move up 10mg every other day, until hitting 80mg/daily. At that point, you will be reassessed by a Nurse or the Clinic Physician, and allowed to continue going upwards at a rate of 5-10mg every other day, until you reach a dose at which you feel is sufficient - Minimal cravings with minimal sedation/side effects.

Clinics are usually closed on Sunday; so you'll receive your sunday dose on saturday in a take home bottle with your name/dose printed on the side.

You must return the empty bottle on monday in order to receive your next dose - Otherwise you'll be written up and put on clinic probation for 6 months or so.
Each week period that you succesfully follow all the rules and have returned your take home bottles, you'll usually gain 1 additional take-home day each week. Therefore, after 6 weeks of full compliance, you'll only need to show up at the clinic once weekly, and so on - A maximum of 30 days take-home supply are permitted by federal law.

Once you're showing up to the clinic only once every few weeks to receive your take homes, It is likely that you'll be given methadone in the tablet form, large 40mg dispersable disks which you dissolve in water, like an alka seltzer.

Friday, January 7, 2011


MDxx refers to a class of substituted methylenedioxyphenethylamines. MDMA (ecstasy) is the prototypical compound of this series - as such, drugs of the MDxx series are considered analogues of MDMA. Not all of these compounds are explicitly listed as controlled substances. Some have been, and continue to be, available as recreational research compounds for casual use.

MDPEA (3,4-methylenedioxyphenethylamine)
Compounds of this class are all built from a substituted phenethylamine moeity, containing a methylenedioxy group (a carbene group attatched with 2 oxygen atoms) off of the benzene ring - this base compound is known as 3,4-methylenedioxy-phenethylamine, or MDPEA.

Popular drugs of this series include MDMA, MDA, MDPEA, MDPV, MDAI, MDEA, and bk-MDMA; a few of which are now controlled substances in the US, and a few which may not yet be.

MDxx compounds are generally taken as recreational or party drugs. They produce a range of sympathomimetic (i.e. stimulant), euphorigenic, empathogenic, and psychedelic effects similar to ecstasy and amphetamine.

Considering MDMA as a prototype, MDxx compounds produce their desired effects by increasing extracellular concentrations of the monoamine neurotransmitters in the brain (dopamine, norepinephrine, and 5HT), this is being done by various means, including reuptake inhibition and transport phosphorylation.

The empathogen properties set many of these compounds apart from psychedelics such as LSD or DMT, and from traditional stimulants like amphetamine; these effects, marked by increased empathy, sociability, and affection, have been linked with the reversed out-pouring of 5HT into synaptic terminals (i.e. 5HT phosphorylation) - MDMA is a relatively potent serotonin releasing agent - as opposed to hallucinogens such as LSD which only bind and activate serotonergic receptors, or as opposed to stimulants like amphetamine, which don't exhibit nearly this degree of serotonergic action. MDMA also produces weak activation of the 5HT receptor, and its serotonergic properities are believed to induce increased active levels of the hormone & neuromodulator oxytocin.